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Cholecystokinin-33 (CCK-33) attenuates short-term food foraging, hoarding, and intake in Siberian hamsters
T.H. Moran / Appetite 51 (2010) 350–412
Body mass loss during adaptation to short winter-like days does not affect food foraging or hoarding B.J.W. TEUBNER ∗ , T.J. BARTNESS. Georgia State University, Atlanta, USA Siberian hamsters are a seasonal species that exhibits a wide range of physiological and behavioral alterations depending chiefly upon the photoperiod including a reduction in body mass in short ‘winter-like’ days (SD) of ∼25–45%. We previously showed that food deprived hamsters lose body mass and, upon refeeding, increase food foraging and hoarding. Siberian hamsters that have attained their final SD stable body mass do not increase food hoarding. Therefore, it may be that only when body mass is dynamically decreasing, might food foraging and hoarding increase, as it does when they are fasted. Therefore, we asked: Does the initial body mass loss with SD exposure increase food foraging and hoarding? Hamsters were housed in a simulated burrow equipped with a wheel running-based foraging system to deliver food pellets in either long ‘summer-like’ days (LD) or SDs for 8 weeks. Food foraging, hoarding and intake were measured daily. Despite a significant reduction in body mass over the 8 weeks in SD, foraging and hoarding did not change and food intake showed the normal SD decrease. Hoarding in SDs was significantly decreased compared with hamsters maintained in LDs at weeks 3–6. Therefore, the SD-induced decreased body mass does not trigger increased food foraging or hoarding, unlike other body mass reducing challenges. Acknowledgments: Funded by NIH R01 and DK 78358. doi:10.1016/j.appet.2008.04.241
Cholecystokinin-33 (CCK-33) attenuates short-term food foraging, hoarding, and intake in Siberian hamsters B.J.W. TEUBNER ∗ , T.J. BARTNESS. Georgia State University, Atlanta, USA Neurochemicals that stimulate food foraging and hoarding in Siberian hamsters are becoming more apparent, but we do not know if cessation of these behaviors is due to waning of excitatory stimuli and/or the advent of inhibitory factors. Cholecystokinin (CCK) may be such an inhibitory factor as it is physiologically important in decreasing food intake in several species including Siberian hamsters. CCK-33 is the most prevalent form of circulating CCK and its systemic injection in rats decreases food intake, doing so to a greater extent than CCK-8. We found minimal effects of CCK8 on food foraging and hoarding previously in Siberian hamsters, but have not tested CCK-33. Therefore, we asked: Does CCK-33 decrease normal levels or food deprivation-induced increases in food foraging, hoarding and intake? Hamsters were housed in a wheel running-based foraging system with simulated burrows to test the effects of peripheral injections (1 ml) of CCK-33 (13.2, 26.4, or 52.8 g/kg body mass), with or without a preceding 56 h food deprivation. The highest dose of CCK-33 caused large baseline reductions in all three behaviors for the 1st hour post-injection compared with saline; in addition, the medium CCK-33 dose was sufficient to curtail food intake and foraging during the 1st hour. In food deprived hamsters, the highest CCK-33 dose decreased food intake and hoarding almost completely compared with saline controls. Therefore, CCK-33 appears to be a potent inhibitor of food intake, hoarding, and foraging in both ad libitum and food deprived hamsters. Acknowledgments: Funded by NIH R01 DK 78358. doi:10.1016/j.appet.2008.04.242
405
Protein-induced satiety D. TOME . AgroParisTech, INRA, UMR914, Paris, France Dietary protein generates signals involved in the induction of satiety. They associate amino acids, gut neuropeptides and hormones acting on specific area involved in the control of food intake in the brain either through vagus-mediated pathways as well as directly after their release in the peripheral blood. Protein infused in the duodenum are able to generate vagal afferent activation in the rat, mainly through a cholecystokinin-dependent mechanism. Amino acid sensors in the hepato-portal region were also shown to modulate the activity of hepatic vagal afferent fiber. Ingestion of protein activates Fos more than other nutrients in the Nucleus of the Tractus Solitarii through a vagus-mediated pathway. This is associated to the activation of noradrenergic/adrenergic pathway known to be involved in cholecystokinin-induced satiety. In contrast there is no activation of the glucagon like peptide 1 (GLP1) pathway, which is triggered during aversive-induced anorexia. Ingestion of protein also activates satiety pathway in the Arcuate Nucleus of the Hypothalamus, characterized by an up-regulation of the melanocortin (␣-MSH containing neurons) POMC pathway and a down-regulation of the neuropeptide Y NPY pathway. Amino acid sensitive neurons have been detected in the lateral hypothalamus (LHA). A critical role for peptide YY in protein-mediated satiation and body-weight regulation has also been proposed. A central role for hypothalamic neuronal AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) have also been proposed in protein-induced satiety. Lastly protein induced lower activation of GABA and opioid neurons by a protein meal in the accubens nucleus. doi:10.1016/j.appet.2008.04.243
In vitro evidence of a computational model for switching between ingestion and rejection J.B. TRAVERS 1,∗ , J. NASSE 1 , R. ROGERS 2 , S. VENUGOPAL 1 , D. TERMAN 3 . 1 Ohio State University, Columbus, USA 2 Pennington Biomedical Research Center, Baton Rouge, USA 3 Ohio State University, Department of Mathematics, Columbus, USA The lower brainstem contains the neural circuitry to switch between oromotor patterns of ingestion (licking) and rejection (gaping) based on taste. We have developed a computational model of this switching mechanism using Hodgkin Huxley formalism and three classes of pre-oromotor neurons (Venugopal et al., 2007). We now present data in support of this model using calcium imaging and whole-cell patch clamp recording from identified preoromotor neurons in the reticular formation (RF) to show that disinhibition is a viable mechanism for amplitude changes between licks and gapes. The infusion of GABAA antagonists increased the magnitude of Ca2+ flux from RF neurons in response to electrical stimulation of the rostral (gustatory) solitary nucleus (rNST) in a slice preparation. Whole cell patch clamp recording further revealed inhibitory currents in RF neurons that were suppressed by rNST stimulation concomitant with increased excitatory currents in the same cell. We further demonstrated both mono- and polysynaptic excitatory currents in RF cells from rNST stimulation that might initiate licking behavior, and polysynaptic GABAA inhibitory currents. The model predicts that differences in the decay kinetics of two inhibitory neurotransmitters such as those found between GABA and glycine can change the EMG pattern from licks to gapes, and we are presently exploring the effects of glycine on identified neurons in vitro. Acknowledgments: Supported by DC00417 (JBT) and NSF DMS0514356 (DT). doi:10.1016/j.appet.2008.04.244
Body mass loss during adaptation to short winter-like days does not affect food foraging or hoarding B.J.W. TEUBNER ∗ , T.J. BARTNESS. Georgia State University, Atlanta, USA Siberian hamsters are a seasonal species that exhibits a wide range of physiological and behavioral alterations depending chiefly upon the photoperiod including a reduction in body mass in short ‘winter-like’ days (SD) of ∼25–45%. We previously showed that food deprived hamsters lose body mass and, upon refeeding, increase food foraging and hoarding. Siberian hamsters that have attained their final SD stable body mass do not increase food hoarding. Therefore, it may be that only when body mass is dynamically decreasing, might food foraging and hoarding increase, as it does when they are fasted. Therefore, we asked: Does the initial body mass loss with SD exposure increase food foraging and hoarding? Hamsters were housed in a simulated burrow equipped with a wheel running-based foraging system to deliver food pellets in either long ‘summer-like’ days (LD) or SDs for 8 weeks. Food foraging, hoarding and intake were measured daily. Despite a significant reduction in body mass over the 8 weeks in SD, foraging and hoarding did not change and food intake showed the normal SD decrease. Hoarding in SDs was significantly decreased compared with hamsters maintained in LDs at weeks 3–6. Therefore, the SD-induced decreased body mass does not trigger increased food foraging or hoarding, unlike other body mass reducing challenges. Acknowledgments: Funded by NIH R01 and DK 78358. doi:10.1016/j.appet.2008.04.241
Cholecystokinin-33 (CCK-33) attenuates short-term food foraging, hoarding, and intake in Siberian hamsters B.J.W. TEUBNER ∗ , T.J. BARTNESS. Georgia State University, Atlanta, USA Neurochemicals that stimulate food foraging and hoarding in Siberian hamsters are becoming more apparent, but we do not know if cessation of these behaviors is due to waning of excitatory stimuli and/or the advent of inhibitory factors. Cholecystokinin (CCK) may be such an inhibitory factor as it is physiologically important in decreasing food intake in several species including Siberian hamsters. CCK-33 is the most prevalent form of circulating CCK and its systemic injection in rats decreases food intake, doing so to a greater extent than CCK-8. We found minimal effects of CCK8 on food foraging and hoarding previously in Siberian hamsters, but have not tested CCK-33. Therefore, we asked: Does CCK-33 decrease normal levels or food deprivation-induced increases in food foraging, hoarding and intake? Hamsters were housed in a wheel running-based foraging system with simulated burrows to test the effects of peripheral injections (1 ml) of CCK-33 (13.2, 26.4, or 52.8 g/kg body mass), with or without a preceding 56 h food deprivation. The highest dose of CCK-33 caused large baseline reductions in all three behaviors for the 1st hour post-injection compared with saline; in addition, the medium CCK-33 dose was sufficient to curtail food intake and foraging during the 1st hour. In food deprived hamsters, the highest CCK-33 dose decreased food intake and hoarding almost completely compared with saline controls. Therefore, CCK-33 appears to be a potent inhibitor of food intake, hoarding, and foraging in both ad libitum and food deprived hamsters. Acknowledgments: Funded by NIH R01 DK 78358. doi:10.1016/j.appet.2008.04.242
405
Protein-induced satiety D. TOME . AgroParisTech, INRA, UMR914, Paris, France Dietary protein generates signals involved in the induction of satiety. They associate amino acids, gut neuropeptides and hormones acting on specific area involved in the control of food intake in the brain either through vagus-mediated pathways as well as directly after their release in the peripheral blood. Protein infused in the duodenum are able to generate vagal afferent activation in the rat, mainly through a cholecystokinin-dependent mechanism. Amino acid sensors in the hepato-portal region were also shown to modulate the activity of hepatic vagal afferent fiber. Ingestion of protein activates Fos more than other nutrients in the Nucleus of the Tractus Solitarii through a vagus-mediated pathway. This is associated to the activation of noradrenergic/adrenergic pathway known to be involved in cholecystokinin-induced satiety. In contrast there is no activation of the glucagon like peptide 1 (GLP1) pathway, which is triggered during aversive-induced anorexia. Ingestion of protein also activates satiety pathway in the Arcuate Nucleus of the Hypothalamus, characterized by an up-regulation of the melanocortin (␣-MSH containing neurons) POMC pathway and a down-regulation of the neuropeptide Y NPY pathway. Amino acid sensitive neurons have been detected in the lateral hypothalamus (LHA). A critical role for peptide YY in protein-mediated satiation and body-weight regulation has also been proposed. A central role for hypothalamic neuronal AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) have also been proposed in protein-induced satiety. Lastly protein induced lower activation of GABA and opioid neurons by a protein meal in the accubens nucleus. doi:10.1016/j.appet.2008.04.243
In vitro evidence of a computational model for switching between ingestion and rejection J.B. TRAVERS 1,∗ , J. NASSE 1 , R. ROGERS 2 , S. VENUGOPAL 1 , D. TERMAN 3 . 1 Ohio State University, Columbus, USA 2 Pennington Biomedical Research Center, Baton Rouge, USA 3 Ohio State University, Department of Mathematics, Columbus, USA The lower brainstem contains the neural circuitry to switch between oromotor patterns of ingestion (licking) and rejection (gaping) based on taste. We have developed a computational model of this switching mechanism using Hodgkin Huxley formalism and three classes of pre-oromotor neurons (Venugopal et al., 2007). We now present data in support of this model using calcium imaging and whole-cell patch clamp recording from identified preoromotor neurons in the reticular formation (RF) to show that disinhibition is a viable mechanism for amplitude changes between licks and gapes. The infusion of GABAA antagonists increased the magnitude of Ca2+ flux from RF neurons in response to electrical stimulation of the rostral (gustatory) solitary nucleus (rNST) in a slice preparation. Whole cell patch clamp recording further revealed inhibitory currents in RF neurons that were suppressed by rNST stimulation concomitant with increased excitatory currents in the same cell. We further demonstrated both mono- and polysynaptic excitatory currents in RF cells from rNST stimulation that might initiate licking behavior, and polysynaptic GABAA inhibitory currents. The model predicts that differences in the decay kinetics of two inhibitory neurotransmitters such as those found between GABA and glycine can change the EMG pattern from licks to gapes, and we are presently exploring the effects of glycine on identified neurons in vitro. Acknowledgments: Supported by DC00417 (JBT) and NSF DMS0514356 (DT). doi:10.1016/j.appet.2008.04.244